Abstract

Friday, October 21, 2016

A means to slow Alzheimer's?

This past
Sunday, the Boston Globe ran a
lengthy article devoted to an Eli Lilly drug candidate designed to slow—not
cure—Alzheimer’s disease. The article, produced by the news organization STAT, stated
that while the drug failed to slow mental and physical deterioration among people
with mild-to-moderate Alzheimer’s, the news was not all bad. As the author of
the piece, Damian Garde, noted, “a secondary analysis of pooled data in
patients with mild forms of the disease” showed a 34 percent reduction in the
patients’ cognitive decline.

This finding could be significant. While some people with
Alzheimer’s deteriorate rapidly, the much more common scenario is a long, gradual
decline—so mild that in the earliest stage of the disease, neither doctors nor
patients are likely to be aware that the person has the disease. This is
especially true for people with early-onset Alzheimer’s, because they aren’t at
an age when the disease is expected to occur, and symptoms are mistaken for
other problems, such as attention deficit disorder. In my case, it took about three
years from my first symptoms to my diagnosis. Like most people in my situation,
I felt that I had been given a death sentence. And I had. But the executioner
has turned out to be a lazy fellow, and four-and-one-half years later, my
symptoms remain mild.

But there is a possibility that Eli Lilly’s drug
candidate, solanezumab, could add many additional years to the arc of
Alzheimer’s progression. At the far end of optimism is the notion that
Alzheimer’s could become a manageable disease, as AIDS did in the early 1990s,
thanks to a complex cocktail of drugs. According to Garde, people treated with solanezumab
performed about 35 percent better on cognitive tests than those on a placebo.

In tandem with common-sense measures such as exercising
regularly, following a reasonable diet and getting plenty of sleep, solanezumab
could extend life expectancy significantly in the face of Alzheimer’s,
according to Garde. But as he noted, roughly 99 percent of all Alzheimer’s
treatments have failed. A particularly blunt statement came from Mayo Clinic
neurologist David Knopman: “I hate having to tell people that we don’t have
anything that can truly arrest the disease at this point.” The rather modest
aim, according to Garde, is to see if the drug does better than the placebo. The
plan is to inject the subjects, all of whom are at a relatively mild stage of Alzheimer’s,
once a month with a drug that has the potential to clear away amyloid plaque, a
dominant feature of the disease.

As the Alzheimer’s researcher Dr. Howard Fillit commented
in Garde’s article, the best-case scenario would be that solanezumab would
serve as a foundation for further Alzheimer’s research. That, Fillit said,
would likely create the biggest market for any pharmaceutical ever. Under
optimal circumstances, the drug could be approved by late next year. That
strikes me as a long shot. Still, solanezumab is welcome news.